Cyclosporine is a potent immunosuppressive agent and is a mainstay of anti-rejection therapy in adult and pediatric heart transplant recipients. However, cyclosporine-induced hypertension remains a major complication of cyclosporine use, and may occur in up to 96% of pediatric cardiac transplant patients. Cyclosporine-induced hypertension is particularly refractory therapy, and multiple antihypertensive medications have been used with limited success. The cellular mechanism of cyclosporine induced hypertension remains unknown. Recent in vitro studies have suggested that cyclosporine has a direct effect on peripheral vasculature to decrease the production of endothelium-derived nitric oxide, a potent vasodilator, leading to impaired vascular smooth muscle relaxation, elevation of systemic vascular resistance, and subsequent systemic hypertension. The aim of the proposed study is to test the typothesis that cyclosporine-induced hypertension in vivo is secondary to decreased endothelial production of nitric oxide. To test this hypothesis, we will investigate the acute effects of intravenous administration of L-arginine, the amino acid precursor to nitric oxide, in pediatric cardiac transplant recipients treated with cyclosporine.